Actin Structure in Fibroblasts

Striking changes in actin cytoarchitecture occur when cultured fibroblasts become oncogenically transformed by tumor viruses. These changes were first observed by electron and immunofluorescence miscroscopy as a loss of large bundles of actin microfilaments called “stress fibers.” Recent technical innovations for visualizing the cytoskeleton have revealed that actin structure in normal fibroblasts is much more complex than was originally supposed and that the changes in actin structure that occur on transformation, collectively referred to as “the actin transformation,” are manifold. In cells transformed by certain DNA- and RNA-containing tumor viruses, these actin alterations have been shown to be the consequence of specific viral genes that simultaneously set in motion a variety of pleiotypic changes in the infected cell and that are also required for tumorigenicity. Several of these transforming genes code for proteins that may directly induce transformation and tumorigenesis. Considerable progress has been made in recent years toward the identification of these proteins. Although the transforming proteins encoded by different viruses are distinct, they share certain properties that may be important in bringing about the actin transformation. Furthermore, since transformation induced by these distinct tumor viruses results in a more or less common actin phenotype in the infected cell, it is likely that the actin transformation contributes to the common features of transformation and tumorigenicity. Indeed, a wealth of studies have accumulated that show correlations among the actin transformation, tumorigenicity, and individual transformation parameters, some of which are related to growth control and others of which are not obviously growth-related. Nonetheless, a cause-and-effect relationship has not been demonstrated between the actin transformation and any of these parameters.